ArticleMolecular and cellular biology1995
A new class of histone H2A mutations in Saccharomyces cerevisiae causes specific transcriptional defects in vivo.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 108 citations in OpenAlex.
- A tale of two serines: the effects of histone H2A mutations S122A and S129A on chromosome nondisjunction in Saccharomyces cerevisiae.Genetics · 2025Article
- DNA Damage-Induced Phosphorylation of Histone H2A at Serine 15 Is Linked to DNA End Resection.Molecular and cellular biology · 2021Article
- The related coactivator complexes SAGA and ATAC control embryonic stem cell self-renewal through acetyltransferase-independent mechanisms.Cell reports · 2021Article
- Live-cell single particle imaging reveals the role of RNA polymerase II in histone H2A.Z eviction.eLife · 2020Article
- Article
- SAGA Is a General Cofactor for RNA Polymerase II Transcription.Molecular cell · 2017Article
- Interaction of the Jhd2 Histone H3 Lys-4 Demethylase with Chromatin Is Controlled by Histone H2A Surfaces and Restricted by H2B Ubiquitination.The Journal of biological chemistry · 2015Article
- Feedback Control of Snf1 Protein and Its Phosphorylation Is Necessary for Adaptation to Environmental Stress.The Journal of biological chemistry · 2015Article
- H2A histone-fold and DNA elements in nucleosome activate SWR1-mediated H2A.Z replacement in budding yeast.eLife · 2015Article
- Histone proteolysis: a proposal for categorization into 'clipping' and 'degradation'.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
- The SAGA coactivator complex acts on the whole transcribed genome and is required for RNA polymerase II transcription.Genes & development · 2014Article
- Article
- DNA replication origin function is promoted by H3K4 di-methylation in Saccharomyces cerevisiae.Genetics · 2012Article
- An integrated genomic approach identifies ARID1A as a candidate tumor-suppressor gene in breast cancer.Oncogene · 2012Article
- Chromatin and transcription in yeast.Genetics · 2012Review
- Role of histone tails in structural stability of the nucleosome.PLoS computational biology · 2011Article
- A genetic and molecular toolbox for analyzing histone ubiquitylation and sumoylation in yeast.Methods (San Diego, Calif.) · 2011Review
- Article
- NuA4-dependent acetylation of nucleosomal histones H4 and H2A directly stimulates incorporation of H2A.Z by the SWR1 complex.The Journal of biological chemistry · 2010Article
- Alterations in DNA replication and histone levels promote histone gene amplification in Saccharomyces cerevisiae.Genetics · 2010Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Nucleosomes have been shown to repress transcription both in vitro and in vivo. However, the mechanisms by which this repression is overcome are only beginning to be understood. Recent evidence suggests that in the yeast Saccharomyces cerevisiae, many transcriptional activators require the SNF/SWI complex to overcome chromatin-mediated repression. We have identified a new class of mutations in the histone H2A-encoding gene HTA1 that causes transcriptional defects at the SNF/SWI-dependent gene SUC2. Some of the mutations are semidominant, and most of the predicted amino acid changes are in or near the N- and C-terminal regions of histone H2A. A deletion that removes the N-terminal tail of histone H2A also caused a decrease in SUC2 transcription. Strains carrying these histone mutations also exhibited defects in activation by LexA-GAL4, a SNF/SWI-dependent activator. However, these H2A mutants are phenotypically distinct from snf/swi mutants. First, not all SNF/SWI-dependent genes showed transcriptional defects in these histone mutants. Second, a suppressor of snf/swi mutations, spt6, did not suppress these histone mutations. Finally, unlike in snf/swi mutants, chromatin structure at the SUC2 promoter in these H2A mutants was in an active conformation. Thus, these H2A mutations seem to interfere with a transcription activation function downstream or independent of the SNF/SWI activity. Therefore, they may identify an additional step that is required to overcome repression by chromatin.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.